Chapter 18: THE HEART.

Chapter 18: THE HEART

Heart Anatomy Approximately the size of a fist Location
In the mediastinum between second rib and fifth intercostal space On the superior surface of diaphragm Two-thirds to the left of the midsternal line Anterior to the vertebral column, posterior to the sternum Enclosed in pericardium, a double-walled sac

Midsternal line 2nd rib Sternum Diaphragm Point of maximal intensity
(PMI) (a) Figure 18.1a

Superior Aorta vena cava Parietal pleura (cut) Pulmonary Left lung
trunk Left lung Pericardium (cut) Apex of heart Diaphragm (c) Figure 18.1c

Pericardium 3 layers Fibrous pericardium (superficial)
Serous pericardium (2 layers) Parietal layer Visceral layer lines the internal surface of the fibrous pericardium Visceral layer (epicardium) on external surface of the heart

Pericardium: Layer Functions
Fibrous layer Protects, anchors, and prevents overfilling Serous parietal layer lines the internal surface of the fibrous pericardium Parietal means relating to or forming the wall of a body part, organ, or cavity Serous visceral layer on external surface of the heart, known as the epicardium Visceral means organs

Percardium: Layer Functions
The parietal and visceral serous pericardium form a sac or cushion of space around the heart This sac is called the pericardial cavity Filled with fluid Purpose = decrease friction

Pulmonary Fibrous pericardium trunk Parietal layer of
Figure 18.2 Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Epicardium (visceral layer of serous pericardium) Myocardium Endocardium Pulmonary trunk Heart chamber Heart wall Pericardium

Layers of the Heart Wall
Epicardium—visceral layer of the serous pericardium

Myocardium Myo = muscle Spiral bundles of cardiac muscle cells Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue Anchors cardiac muscle fibers Supports great vessels and valves Limits spread of action potentials to specific paths

Endocardium is continuous with endothelial lining of blood vessels

Pulmonary Fibrous pericardium trunk Parietal layer of
Figure 18.2 Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Epicardium (visceral layer of serous pericardium) Myocardium Endocardium Pulmonary trunk Heart chamber Heart wall Pericardium

Cardiac muscle bundles Figure 18.3

Chambers Four chambers
Two atria (receiving chambers) and two ventricles (discharging chambers) Left and right atrium, left and right ventricle Coronary sulcus (atrioventricular groove, AV groove) encircles the junction of the atria and ventricles Sulcus = deep, narrow groove Auricles (ears) increase atrial volume

Two ventricles (discharging chambers)
Separated by the interventricular septum Pumping chambers R ventricle pumps blood into the lungs L ventricle pumps blood into the body Inter = between Intra = within

Direction of blood flow
A note on vessels Direction of blood flow Artery = Away from the heart Vein = to the heart This is important to remember when looking at the heart; arteries do not always carry oxygenated blood and veins do not always carry deoxygenated blood i.e., pulmonary artery carries deoxygenated blood Pulmonary veins carry oxygenated blood

Brachiocephalic trunk Left subclavian artery Superior vena cava
Left common carotid artery Brachiocephalic trunk Left subclavian artery Superior vena cava Aortic arch Right pulmonary artery Left pulmonary artery Ascending aorta Left pulmonary veins Pulmonary trunk Right pulmonary veins Auricle of left atrium Right atrium Left coronary artery (in coronary sulcus) Right coronary artery (in coronary sulcus) Left ventricle Right ventricle Great cardiac vein Inferior vena cava Apex (b) Anterior view Figure 18.4b

(d) Posterior surface view Aorta Left pulmonary artery
Figure 18.4d (d) Posterior surface view Aorta Left pulmonary artery veins Auricle of left atrium Left atrium Great cardiac vein Posterior vein of left ventricle Left ventricle Apex Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium Inferior vena cava Right coronary artery (in coronary sulcus) Coronary sinus Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein Right ventricle

Atria: The Receiving Chambers
Walls are ridged by pectinate muscles Vessels entering right atrium Superior vena cava Inferior vena cava Coronary sinus Vessels entering left atrium Right and left pulmonary veins

Ventricles: The Discharging Chambers
Walls are ridged by trabeculae carneae Papillary muscles project into the ventricular cavities (anchor valves) Vessel leaving the right ventricle Pulmonary trunk Vessel leaving the left ventricle Aorta

Aorta Left pulmonary artery Left atrium veins Mitral (bicuspid) valve
Figure 18.4e Aorta Left pulmonary artery Left atrium veins Mitral (bicuspid) valve Aortic valve Pulmonary valve Left ventricle Papillary muscle Interventricular septum Epicardium Myocardium Endocardium (e) Frontal section Superior vena cava Right pulmonary Pulmonary trunk Right atrium Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava

Pathway of Blood Through the Heart
The heart is two side-by-side pumps Right side is the pump for the pulmonary circuit Vessels that carry blood to and from the lungs Left side is the pump for the systemic circuit Vessels that carry the blood to and from all body tissues

Capillary beds of lungs where gas exchange occurs Pulmonary Circuit
Pulmonary veins Pulmonary arteries Aorta and branches Venae cavae Left atrium Left ventricle Right atrium Heart Right ventricle Systemic Circuit Oxygen-rich, CO2-poor blood Capillary beds of all body tissues where gas exchange occurs Oxygen-poor, CO2-rich blood Figure 18.5

Right atrium Right ventricle Pulmonary trunk Pulmonary arteries Lungs Pulmonary veins Left atrium Left ventricle Aorta Systemic circulation

Pulmonary circuit is a short, low-pressure circulation Systemic circuit blood encounters much resistance in the long pathways As a result, the left ventricle has a much thicker wall (stronger muscle)

Left ventricle Right ventricle Interventricular septum Figure 18.6

Heart Valves

Heart Valves Ensure unidirectional blood flow through the heart
Atrioventricular (AV) valves (balloons) Prevent backflow into the atria when ventricles contract Tricuspid valve (right) Between R atrium and R ventricle Mitral valve (left) Between L atrium and L ventricle Chordae tendineae anchor AV valve cusps to papillary muscles

Semilunar (SL) valves (cups)
Heart Valves Semilunar (SL) valves (cups) Prevent backflow into the ventricles when ventricles relax Pulmonary valve between R ventricle and pulmonary trunk Aortic valve Between L ventricle and aorta

Aorta Left pulmonary artery Superior vena cava Right pulmonary artery
Left atrium Left pulmonary veins Pulmonary trunk Right atrium Mitral (bicuspid) valve Right pulmonary veins Aortic valve Pulmonary valve Tricuspid valve Left ventricle Right ventricle Papillary muscle Chordae tendineae Interventricular septum Trabeculae carneae Epicardium Inferior vena cava Myocardium Endocardium (e) Frontal section Figure 18.4e

Blood flow through the heart with valves
Right atrium  tricuspid valve  right ventricle  pulmonary semilunar valve  pulmonary trunk  pulmonary arteries  Lungs  pulmonary veins  left atrium  (mitral) bicuspid valve  left ventricle  aortic semilunar valve  aorta systemic circulation

(right atrioventricular) valve Area of cutaway
Myocardium Pulmonary valve Aortic valve Tricuspid (right atrioventricular) valve Area of cutaway Mitral valve Tricuspid valve Mitral (left atrioventricular) valve Myocardium Tricuspid (right atrioventricular) valve Aortic valve Mitral (left atrioventricular) valve Pulmonary valve Aortic valve Pulmonary valve Aortic valve Pulmonary valve Area of cutaway (b) Fibrous skeleton Mitral valve Tricuspid valve (a) Anterior Figure 18.8a

(right atrioventricular) valve
Myocardium Tricuspid (right atrioventricular) valve Mitral (left atrioventricular) valve Aortic valve Pulmonary valve Pulmonary valve Aortic valve Area of cutaway (b) Mitral valve Tricuspid valve Figure 18.8b

attached to tricuspid valve flap Papillary muscle
Pulmonary valve Aortic valve Area of cutaway Mitral valve Tricuspid valve Chordae tendineae attached to tricuspid valve flap Papillary muscle (c) Figure 18.8c

Opening of inferior vena cava Mitral valve Chordae tendineae
Tricuspid valve Myocardium of right ventricle Myocardium of left ventricle Pulmonary valve Aortic valve Area of cutaway Papillary muscles Mitral valve Interventricular septum Tricuspid valve (d) Figure 18.8d

Physiology of Blood Flow through the Heart

heart fills atria, putting pressure against atrioventricular valves;
Blood returning to the heart fills atria, putting pressure against atrioventricular valves; atrioventricular valves are forced open. 1 Direction of blood flow Atrium Cusp of atrioventricular valve (open) As ventricles fill, atrioventricular valve flaps hang limply into ventricles. 2 Chordae tendineae Atria contract, forcing additional blood into ventricles. 3 Papillary muscle Ventricle (a) AV valves open; atrial pressure greater than ventricular pressure Atrium Ventricles contract, forcing blood against atrioventricular valve cusps. 1 Cusps of atrioventricular valve (closed) Atrioventricular valves close. 2 Blood in ventricle Papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria. 3 (b) AV valves closed; atrial pressure less than ventricular pressure Figure 18.9

(a) Semilunar valves open
Aorta Pulmonary trunk As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves, forcing them open. (a) Semilunar valves open As ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close. (b) Semilunar valves closed Figure 18.10

Heart Sounds AV valves closing (tricuspid and mitral) = lub Semilunar valves closing (pulmonic, aortic) = dub

Coronary Circulation

Coronary Circulation The functional blood supply to the heart muscle itself Arterial supply varies considerably and contains many anastomoses (junctions) among branches

Coronary Circulation Arteries Veins
Right and left coronary (in atrioventricular groove) Veins Small cardiac, anterior cardiac, and great cardiac veins, coronary sinus Coronary sinus is where dexoygenated blood from coronary circulation pools and is returned to venous circulation via the inferior vena cava

(a) The major coronary arteries Left atrium Pulmonary trunk
Figure 18.7a Right ventricle coronary artery atrium Posterior interventricular Anterior Circumflex Left Aorta Anastomosis (junction of vessels) Superior vena cava (a) The major coronary arteries Left atrium Pulmonary trunk

(b) The major cardiac veins
Figure 18.7b Superior vena cava Anterior cardiac veins Great vein Coronary sinus (b) The major cardiac veins

Right pulmonary artery
Aorta Superior vena cava Left pulmonary artery Right pulmonary artery Right pulmonary veins Left pulmonary veins Auricle of left atrium Right atrium Left atrium Inferior vena cava Great cardiac vein Coronary sinus Right coronary artery (in coronary sulcus) Posterior vein of left ventricle Posterior interventricular artery (in posterior interventricular sulcus) Left ventricle Apex Middle cardiac vein Right ventricle (d) Posterior surface view Figure 18.4d

Homeostatic Imbalances
Angina pectoris Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium Cells are weakened Myocardial infarction (heart attack) Prolonged coronary blockage Areas of cell death are repaired with noncontractile scar tissue

Histology of Cardiac Muscle

Microscopic Anatomy of Cardiac Muscle
Cardiac muscle cells are striated, short, fat, branched, and interconnected Connective tissue matrix (endomysium) connects to the fibrous skeleton T tubules are wide but less numerous SR (sarcoplasmic reticulum) is simpler than in skeletal muscle SR stores Ca++, which plays an important part in cardiac cell APs and contraction Numerous large mitochondria Multiple nuclei per cell

Microscopic Anatomy of Cardiac Muscle
Intercalated discs: junctions between cells anchor cardiac cells, cause heart to beat as a functional syncytium (as a group) Desmosomes prevent cells from separating during contraction Gap junctions allow ions to pass; electrically couple adjacent cells

Nucleus Intercalated discs Cardiac muscle cell Gap junctions
Desmosomes (a) Figure 18.11a

Cardiac muscle cell Mitochondrion Intercalated disc Nucleus T tubule
Sarcoplasmic reticulum Z disc Nucleus Sarcolemma I band I band A band (b) Figure 18.11b

Physiology of Cardiac Muscle Contraction

Cardiac Muscle Cells

Cardiac Muscle Contraction
Depolarization opens voltage-gated fast Na+ channels in the sarcolemma Reversal of membrane potential from –90 mV to +30 mV Slow Ca2+ channels open (delayed), about 20% of Ca2+ enters cell this way Depolarization wave in T tubules causes the SR to release Ca2+; 80% of Ca2+ released thru SR Ca2+ surge prolongs the depolarization phase (plateau) K+ channels open and Ca2+ channels close, repolarizing the membrane Ca2+ is pumped back into the SR and ECF

Cardiac Muscle Contraction
Because of influx of Ca2+ from slow Ca2+ channels and the SR, the duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle Skeletal muscle AP is 1-2ms Contraction is ms Cardiac muscle AP is 200ms Contraction is 200ms

Cardiac AP and Ca++ Channel
Ca++ Channel Open Usually 200 mv action potential....drug that blocks calcium cause to pump less……shorter action potential less potential for rhythm issues

1 2 3 Action Depolarization is potential due to Na+ influx through
fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase. 1 Plateau 2 Tension development (contraction) Membrane potential (mV) 1 3 Tension (g) Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. 2 Absolute refractory period Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. 3 Time (ms) Figure 18.12

Cardiac Muscle Physiology
EPI Beta blockers B-1 Adrenergic receptor Adenylate cyclase EPI cAMP Cyclase-a ATP Prot. Kinase CA++ Channels CA++ Influx Prot.Kinase-a Ca++ B1: make heart pump harder…..also open Ca2+ channels….potentiates Na HTN, chronic angina, most common arrhythmias Cross Bridge Formation “Phosphorylation” Tension Generation CA++ Channel Blockers

Heart Conduction System

Heart Physiology: Electrical Events
Intrinsic cardiac conduction system A network of noncontractile cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart The independent but coordinated activity of the heart is a function of Gap junctions Intrinsic conducting system

Cardiac Pacemaker Cells

Found in SA node, AV node, AV bundle, R and L bundle branches, Purkinje fibers; part of conduction system of the heart Autorhythmic cells (1% of cardiac muscle cells) Have unstable RMP (resting membrane potential) Cells continously depolarize because they drift toward threshold Depolarization of the heart is rhythmic and spontaneous Gap junctions ensure the heart contracts as a unit

Unstable resting potentials = pacemaker potential Pacemaker potential is due to slow Na+ channels and closing of K+ channels Slow Na+ channels leak positive ions into the cell, causing the RMP to creep up At threshold, Ca2+ channels open Explosive Ca2+ influx produces the rising phase of the action potential (not Na+) Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels

Action potential Threshold Pacemaker potential 2 2 3 1 1 1 2 3
This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line. 1 Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. 2 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. 3 Figure 18.13

Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node (pacemaker) Generates impulses about 75 times/minute (sinus rhythm) Depolarizes faster than any other part of the myocardium Atrial contraction

Atrioventricular (AV) node Smaller diameter fibers; fewer gap junctions Delays impulses approximately 0.1 second Want a delay between contract of atria and ventricles Depolarizes 50 times per minute in absence of SA node input

Atrioventricular (AV) bundle (bundle of His) Only electrical connection between the atria and ventricles

Right and left bundle branches Two pathways in the interventricular septum that carry the impulses toward the apex of the heart

Purkinje fibers Complete the pathway into the apex and ventricular walls AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

(a) Anatomy of the intrinsic conduction system showing the
Figure 18.14a (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Superior vena cava Right atrium Left atrium Purkinje fibers Inter- ventricular septum 1 The sinoatrial (SA) node (pacemaker) generates impulses. 2 The atrioventricular (AV) node. (AV) bundle 4 The bundle branches 3 The Purkinje fibers 5

Defects in the intrinsic conduction system may result in Arrhythmias: irregular heart rhythms Uncoordinated atrial and ventricular contractions Fibrillation: rapid, irregular contractions; useless for pumping blood because atria, and more importantly ventricles, are not getting filled with blood

Defective SA node may result in Ectopic focus: abnormal pacemaker takes over If AV node takes over, there will be a junctional rhythm (40–60 bpm) Defective AV node may result in Partial or total heart block Few or no impulses from SA node reach the ventricles

Electrocardiography

Electrocardiography Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time Three waves P wave: depolarization of SA node QRS complex: ventricular depolarization T wave: ventricular repolarization

QRS complex Ventricular depolarization Ventricular Atrial
Sinoatrial node Ventricular depolarization Ventricular repolarization Atrial depolarization Atrioventricular node S-T Segment P-Q Interval Q-T Interval Figure 18.16

Atrial depolarization, initiated by the SA node, causes the P wave.
Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 Figure 18.17, step 1

Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 R AV node P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. Figure 18.17, step 2

Repolarization P T Q S Atrial depolarization, initiated by the SA node, causes the P wave. 1 R AV node P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. R P T Q S 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. Figure 18.17, step 3

Ventricular depolarization is complete.
Repolarization P T Q S Ventricular depolarization is complete. 4 Figure 18.17, step 4

Repolarization P T Q S 4 Ventricular depolarization is complete. R P T Q S Ventricular repolarization begins at apex, causing the T wave. 5 Figure 18.17, step 5

Repolarization P T Q S Ventricular depolarization is complete. 4 R P T Q S Ventricular repolarization begins at apex, causing the T wave. 5 R P T Q S Ventricular repolarization is complete. 6 Figure 18.17, step 6

Atrial depolarization, initiated by the SA node, causes the P wave. Q
Repolarization R R P T Q P T S 1 Atrial depolarization, initiated by the SA node, causes the P wave. Q S Ventricular depolarization is complete. 4 AV node R R P T P T Q S With atrial depolarization complete, the impulse is delayed at the AV node. 2 Q S Ventricular repolarization begins at apex, causing the T wave. 5 R R P T P T Q S Q 3 S Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. 6 Ventricular repolarization is complete. Figure 18.17

(a) Normal sinus rhythm.
(b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at beats/min. (c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. (d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

Mechanical Events of the Cardiac Cycle

Mechanical Events: The Cardiac Cycle
Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat Systole—contraction Diastole—relaxation Normal heart rate (HR) = bpm

Two sounds (lub-dub) associated with closing of heart valves
Heart Sounds Two sounds (lub-dub) associated with closing of heart valves First sound occurs as AV valves close and signifies beginning of systole Second sound occurs when semilunar valves close at the beginning of ventricular diastole Heart murmurs: abnormal heart sounds most often indicative of valve problems

Tricuspid valve sounds typically heard in right sternal margin of
Figure 18.19 Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space Aortic valve sounds heard in 2nd intercostal space at right sternal margin Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle

Cardiac Cycle: A Note on Pressure
REMEMBER: Blood will always flow from high pressure to low pressure

Phases of the Cardiac Cycle
Ventricular filling—takes place in mid-to-late diastole AV valves are open 80% of blood passively flows into ventricles Atrial systole occurs, delivering the remaining 20% End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole

Ventricular systole Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open End systolic volume (ESV): volume of blood remaining in each ventricle

Isovolumetric relaxation occurs in early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes semilunar valves and causes brief rise in aortic pressure

(mid-to-late diastole)
Left heart QRS P T P Electrocardiogram Heart sounds 1st 2nd Dicrotic notch Aorta Pressure (mm Hg) Left ventricle Atrial systole Left atrium EDV Ventricular volume (ml) SV ESV Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction Isovolumetric contraction phase Ventricular ejection phase Isovolumetric relaxation Ventricular filling 1 2a 2b 3 Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Early diastole Figure 18.20

Volume of blood pumped by each ventricle in one minute
Cardiac Output (CO) Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by a ventricle with each beat

Regulation of Stroke Volume
SV = EDV – ESV Three main factors affect SV Preload Contractility Afterload

Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart) Cardiac muscle exhibits a length-tension relationship At rest, cardiac muscle cells are shorter than optimal length (as opposed to skeletal muscle fibers which are kept near optimal length) This degree of stretch produces more contractile force Increased venous return distends (stretches) the ventricles and increases contraction force Higher preload = higher SV

Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV Contractility rises when more Ca2+ is released into the ICF via the SR Positive inotropic agents increase contractility Ino = muscle, fiber Ca2+, hormones (thyroxine, glucagon, and epinephrine) Negative inotropic agents decrease contractility Acidosis (increased H+) Increased extracellular K+ Calcium channel blockers

Afterload: pressure that must be overcome for ventricles to eject blood The back pressure that arterial blood exerts on the aortic (80mg) and pulmonary (10mg) valves Hypertension increases afterload, resulting in increased ESV and reduced SV

Regulation of Heart Rate
Positive chronotropic factors increase heart rate Chrono = time Negative chronotropic factors decrease heart rate Can be neural, chemical, or physical factors

Autonomic Nervous System Regulation

Exerts the most important extrinsic controls affecting HR Sympathetic nervous system is activated by emotional or physical stressors Sympathetic nerves release norepinephrine which binds to β1 adrenergic receptors on the heart, causing the pacemaker to fire more rapidly It also increases contractility

Parasympathetic nervous system opposes the sympathetic effects and reduces HR when a stressful situation has passe Parasympathetic-initiated cardiac responses are mediated by Acetylcholine (ACh) ACh hyperpolarizes the membranes by opening K+ channels

At rest, the heart exhibits vagal tone At rest, both SNS and PNS send impulses to SA node, but the dominant influence is inhibitory (PNS) The heart rate is slower than if the vagus nerve was not innervating it

Dorsal motor nucleus of vagus The vagus nerve (parasympathetic)
decreases heart rate. Medulla oblongata Cardio- acceleratory center Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Figure 18.15

Exercise (by skeletal muscle and respiratory pumps; see Chapter 19)
Heart rate (allows more time for ventricular filling) Bloodborne epinephrine, thyroxine, excess Ca2+ Exercise, fright, anxiety Venous return Sympathetic activity Parasympathetic activity Contractility EDV (preload) ESV Stroke volume Heart rate Cardiac output Initial stimulus Physiological response Result Figure 18.22

Chemical Regulation of Heart Rate
Hormones Epinephrine from adrenal medulla increases HR and contractility Thyroxine increases HR and enhances the effects of norepinephrine and epinephrine Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function Electrolyte imbalances pose serious danger to the heart

Other Factors that Influence Heart Rate
Age Gender Exercise Body temperature

Tachycardia: abnormally fast heart rate (>100 bpm) If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation May be desirable result of endurance training

Congestive Heart Failure (CHF)
Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs Caused by Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM)

Ventricular septal defect. The superior part of the inter-
Occurs in about 1 in every 500 births every 1500 births Narrowed aorta every 2000 Ventricular septal defect. The superior part of the interventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger. (a) Coarctation of the aorta. A part of the aorta is narrowed, increasing the workload of the left ventricle. (b) Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles. (c) Figure 18.24

QUESTIONS TO TEST WHAT YOU NOW KNOW!!!

The principle of complementary structure and function is evident when examining the coverings of the heart. In what way is this relationship evident? The pericardium surrounds the heart. The epicardium and visceral layer of the pericardium are synonymous. The pericardial cavity surrounds the heart. The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement. Answer: d. The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement.

Of the following layers of the heart wall, which consumes the most energy?
Epicardium Myocardium Endocardium Visceral pericardium Answer: b. Myocardium

Which of the following structures is an exception to the general principle surrounding blood vessel oxygenation levels? Pulmonary artery Aorta Pulmonary veins Both a and c Answer: d. Both a and c

What purpose does the coronary circuit serve?
None; it is a vestigial set of vessels. It delivers 1/20 of the body’s blood supply to the heart muscle itself. It delivers blood to the anterior lung surface for gas exchange. It feeds the anterior thoracic wall. Answer: b. It delivers 1/20 of the body’s blood supply to the heart muscle itself.

right atrium; right ventricle; tricuspid valve
A heart murmur would be detected when blood is heard flowing from the ________ to the __________ through the ___________. right atrium; right ventricle; tricuspid valve right atrium; left atrium; tricuspid valve left ventricle; left atrium; mitral valve left atrium; left ventricle; mitral valve Answer: d. left atrium; left ventricle; mitral valve

contractile myofibril desmosome functional syncytium
The presence of intercalated discs between adjacent cardiac muscle cells causes the heart to behave as a _____________. single chamber contractile myofibril desmosome functional syncytium Answer: d. functional syncytium

The cells are each innervated by a nerve ending.
Cardiac muscle cells have several similarities with skeletal muscle cells. Which of the following is not a similarity? The cells are each innervated by a nerve ending. The cells store calcium ions in the sarcoplasmic reticulum. The cells contain sarcomeres. The cells become depolarized when sodium ions enter the cytoplasm. Answer: a. The cells are each innervated by a nerve ending.

an increased potassium permeability. an influx of calcium ions.
The plateau portion of the action potential in contractile cardiac muscle cells is due to: an increased potassium permeability. an influx of calcium ions. an influx of sodium ions. exit of calcium ions from the sarcoplasmic reticulum. Answer: b. an influx of calcium ions.

a neuromuscular junction a pacemaker potential
The stimulus for the heart’s rhythmic contractions comes from _________. intercalated discs acetylcholine a neuromuscular junction a pacemaker potential Answer: d. a pacemaker potential

The major ionic change that initiates the rising phase of the autorhythmic cell action potential is __________. potassium ion exit sodium ion entry calcium ion entry calcium ion exit Answer: c. calcium ion entry

For which type of heart condition might a doctor prescribe calcium channel blockers?
Depressed heart rate Heart irritability Heart murmur Weak heart rate Answer: b. Heart irritability

Atrioventricular node Atrioventricular bundle Purkinje fibers
In a normal heart, which of the following structures is responsible for setting the heart’s pace? Sinoatrial node Atrioventricular node Atrioventricular bundle Purkinje fibers Answer: a. Sinoatrial node

There would continue to be a normal sinus rhythm.
Predict the nature of an ECG recording when the atrioventricular node becomes the pacemaker. There would continue to be a normal sinus rhythm. The P wave would be much larger than normal. The rhythm would be slower. The T wave would be much smaller than normal. Answer: c. The rhythm would be slower.

sinoatrial node and atrioventricular node Purkinje fibers
The primary input to the heart by the cardioinhibitory center is primarily found in the ___________. sinoatrial node and atrioventricular node Purkinje fibers the cardiac contractile fibers bundle of His Answer: a. sinoatrial node and atrioventricular node

The “lub-dup” heart sounds are produced by:
the walls of the atria and ventricles slapping together during a contraction. the blood hitting the walls of the ventricles and arteries, respectively. the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”). the closing of the semilunar valves (“lub”) and the closing of the atrioventricular valves (“dup”). Answer: c. the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”).

Atrial systole occurs _______ the firing of the sinoatrial node.
before after simultaneously with alternately with Answer: b. after

The majority (80%) of ventricular filling occurs ___________.
during late ventricular systole passively through blood flow alone with atrial systole both a and b Answer: d. both a and b

The atria need that time to prepare for the next contraction.
In terms of blood flow, why is it important that atrial diastole occurs just as ventricular systole begins? Blood is continually propelled in a forward motion down its pressure gradient. The atria need that time to prepare for the next contraction. Ventricular systole pulls the remaining 20% of blood volume from the atria. Blood would flow too fast otherwise. Answer: a. Blood is continually propelled in a forward motion down its pressure gradient.

Cardiac output is determined by________.
heart rate stroke volume cardiac reserve both a and b Answer: d. both a and b

It would remain constant. ESV is not affected by contraction force.
Predict what would happen to the end systolic volume (ESV) if contraction force were to increase. It would decrease. It would increase. It would remain constant. ESV is not affected by contraction force. Answer: a. It would decrease.

the heart expands during inhalation.
The Frank-Starling law of the heart can be demonstrated when an individual takes a deep breath. This is because: the heart expands during inhalation. the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle. sympathetic impulses are sent to the heart during inspiration. both a and c occur. Answer: b. the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle.

because you were startled.
Your heart seems to “pound” after you hear a sudden, loud noise. This increased contractility is: because you were startled. because when a gasp of surprise is emitted, the Frank-Starling law of the heart is evident. due to norepinephrine causing threshold to be reached more quickly. because acetylcholine release is inhibited. Answer: c. due to norepinephrine causing threshold to be reached more quickly.

End diastolic volume is increased. End diastolic volume is decreased.
Predict what happens to end diastolic volume when an increase in heart rate is not accompanied by an increase in contractility. End diastolic volume is increased. End diastolic volume is decreased. End diastolic volume is unchanged. End diastolic volume is not affected by heart rate. Answer: b. End diastolic volume is decreased.

What is the nature of acetylcholine’s inhibitory effect on heart rate?
Acetylcholine induces depolarization in the sinoatrial node. Acetylcholine causes closing of sodium channels in the sinoatrial node. Acetylcholine causes opening of fast calcium channels in contractile cells. Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it. Answer: d. Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it.

Why is high blood pressure damaging to the heart?
With high blood pressure, the blood is more viscous and harder to pump. The heart rate slows down to dangerously low levels if blood pressure is too high. Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood. Sodium concentration increases during high blood pressure and is toxic to the myocardium. Answer: c. Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood.

Chapter 18: THE HEART.

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Chapter 18: THE HEART.

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Presentation on theme: "Chapter 18: THE HEART."— Presentation transcript:

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